The risk of malignant tumor development is increasing in the world. Obesity is an established risk factor for various malignancies. There are many metabolic alterations associated with obesity which promote cancerogenesis. Excessive body weight leads to increased levels of estrogens, chronic inflammation and hypoxia, which can play an important role in the development of malignancies. It is proved that calorie restriction can improve the state of patients with various diseases. Decreased calorie uptake influences lipid, carbohydrate and protein metabolism, hormone levels and cell processes. Many investigations have been devoted to the effects of calorie restriction on cancer development in vitro and in vivo. It was revealed that fasting can regulate the activity of the signal cascades including AMP-activated protein kinase (AMPK), mitogen-activated protein kinase (MAPK), p53, mTOR, insulin/ insulin-like growth factor 1 (IGF1) and JAK-STAT. Up- or down-regulation of the pathways results in the decrease of cancer cell proliferation, migration and survival and the increase of apoptosis and effects of chemotherapy. The aim of this review is to discuss the connection between obesity and cancer development and the mechanisms of calorie restriction influence on cancerogenesis that stress the importance of further research of calorie restriction effects for the inclusion of this approach in clinical practice.

Purpose. Identify the role of ONP rs16944 (-511C/T) of the IL1B gene and rs1143634 (+ 3954 C/T) of the IL1B gene in the development of acute pancreatitis. Material and methods. The study involved 296 people diagnosed with acute pancreatitis. There were 124 (41.89%) males and 172 (58.11%) females. By age, patients ranged from 24 to 83 years old, the average age was 44,3±12,6 years. Patients with mild severity OP - 103 (34.79%) people, moderate severity OP - 110 (37.16%) people, severe severity OP - 83 (28.05%) people. The control group amounted to 78 people. Genomic DNA was isolated by sorption method, the carrier of rs16944 (-511C/T) and rs1143634 (+ 3954C/T) of the IL1B gene was determined by real-time polymerase chain reaction using TaqMan allele discrimination technology and commercially available fluorescence probes. Results. Our study revealed a statistically significant increase in the frequency of carriage of the rs16944 (-511C/T) IL1B gene located in the promoter region of the functional polymorphism, which correlates with the severity of acute pancreatitis. It is known that this polymorphism enhances gene expression and leads to an increase in the level of proinflammatory cytokine. On the other hand, there is no correlation between the presence of the structural polymorphism rs1143634 (+ 3954 C/T), localized in exon 5 of the gene IL1B and the development of the disease, as well as the severity. Conclusions. Thus, it can be assumed that in residents of Krasnoyarsk, the carriage of the rs16944 (-511C/T) ONP gene IL1B is a predictor of the development of acute pancreatitis and severe disease, which coincides with the data obtained when compared with the European population of the NCBI base.

We present modern data on the role of superoxide dismutase (SOD) in antioxidant protection and gene regulation in acute pancreatitis. Antioxidant enzymes are essential in pathogenesis of numerous diseases. SOD is one of the key enzymes of antioxidant system. In this review, we analyzed activity of this enzyme depending on various factors, mechanisms and role in physiological and pathological processes, in particular, acute pancreatitis. SOD is significantly less active in patients with severe acute pancreatitis accompanied by renal failure, severe circulatory disorders and high mortality. There are some SOD gene polymorphisms, in particular, acute destructive pancreatitis R213G, contributing to acute inflammation. Thus, SOD is not only one of the key antioxidant enzymes, but also potential transcription factor regulating activity of signaling pathways. These aspects can underlie new therapies for diseases.

A literature review has been conducted examining the role of single nucleotide polymorphisms of pro-inflammatory factor genes as predictors of risk of developing and severity of acute pancreatitis. The review was conducted on the following databases: Pub Med, Scopus for the period from 2009 to 2021 according to the following keywords: acute pancreatitis, hereditary pancreatitis, severe acute pancreatitis, gene polymorphism, single nucleotide genes, proinflammatory factors. A number of mutations and single nucleotide polymorphisms have been identified, which are the main triggers or cofactors of the initiation of both acute and chronic hereditary pancreatitis. The percentage of cases of idiopathic recurrent acute pancreatitis and idiopathic chronic pancreatitis associated with genetic mutations is 30-60% and 12-43%, respectively. The following genetic variants of the cationic trypsinogen (PRSS1) gene - CFTR, SPINK1 and chymotripsin C (CTRC) - are most often associated with the development of pancreatitis. Inherited pancreatitis associated with gene mutations has SPINK1 autosomal recessive inheritance pattern. When the mutant gene is expressed, the synthesis of a strong trypsin inhibitor prevents premature activation of immature trypsinogen. Data are obtained that IL-6, IL-8, FNOα can activate NF kB transcription factor, inducing, thus, increase in an expression 2 DRIED. It has been found that some COX 2 polymorphisms characterized by increased expression of this enzyme create prerequisites for the progression of the inflammation process, and are possibly predictors of the development of severe acute pancreatitis.

Mutations in the C-KIT gene encoding type III receptor tyrosine kinase that regulates cellular processes, such as differentiation, survival, proliferation, migration, and apoptosis, are found in some neoplasms: gastrointestinal stromal tumor, mastocytosis, melanoma, breast carcinomas, myeloid leukemias, and a number of others. Tumors that exhibit these mutations are sensitive to therapy with tyrosine kinase inhibitors, which makes it necessary to correctly identify the mutation status by C-KIT in order to apply a personalized approach to therapy. This literature review shows that the type and localization of the C-KIT gene mutation are of crucial prognostic value and significance in choosing drugs for antitumor therapy, but traditional diagnostic methods fail to determine accurate mutation characteristics. Routine sequencing techniques focus on identifying the gene mutations associated with specific cellular processes, such as DNA damage and repair. The emergence of next-generation sequencing techniques has solved this problem, making it possible to fully analyze the genome of a malignant neoplasm, with constant screening for new mutations that appear as the tumor develops, affect the prognosis of the disease, and change its sensitivity to the antitumor therapy.